Growth Differentiation Factor 11 is Increased in Patients with Pulmonary Hypertension

Pulmonary arterial hypertension (PAH) is characterised by pulmonary vasoconstriction and vascular remodelling, ultimately leading to heart failure and death. Excessive pulmonary fibroproliferation is the suggested mechanism underlying pathogenesis of PAH. Follistatin-like3 (FSTL3) is a pro-fibrotic inhibitor of the TGF-ß superfamily members and is increased in patients with heart failure (HF). FSTL3 is an inhibitor of Growth-Differentiating Factor-11 (GDF-11). GDF-11 was recently shown to be involved in the development of PAH and vascular remodelling in a rat model. In this pilot study, we aim to determine FSTL3 and GDF-11 mRNA transcripts in polymorphonuclear cells (PMC) from patients with PAH vs those with HF.